Evidence map›Paper›PMID 38195933›Full record

ArticleNature cancer2024

Autotaxin-lysolipid signaling suppresses a CCL11-eosinophil axis to promote pancreatic cancer progression.

Sohinee Bhattacharyya, Chet Oon, Luis Diaz, Holly Sandborg, Erin S Stempinski, Michelle Saoi, Terry K Morgan, Claudia S López, Justin R Cross, Mara H Sherman

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Nature cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  6. Eosinophils in solid cancers: sentinels, predictors, and therapeutic allies.Journal of experimental & clinical cancer research : CR · 2026
    Review
  7. Modulating tumor mechanics and vascular barriers to enhance chemotherapy efficacy in pancreatic tumors and melanoma.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
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  19. High Co-Expression ofBiomedicines · 2025
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Sohinee BhattacharyyaDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA.
Chet OonDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA.
Luis DiazDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA.
Holly SandborgDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA.
Erin S StempinskiMultiscale Microscopy Core Facility, Oregon Health & Science University, Portland, OR, USA.ORCID http://orcid.org/0000-0001-7818-5584
Michelle SaoiDonald B. and Catherine C. Marron Cancer Metabolism Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Terry K MorganDepartment of Pathology, Oregon Health & Science University, Portland, OR, USA.
Claudia S LópezMultiscale Microscopy Core Facility, Oregon Health & Science University, Portland, OR, USA.
Justin R CrossDonald B. and Catherine C. Marron Cancer Metabolism Center, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-6356-057X
Mara H ShermanDepartment of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA. shermam1@mskcc.org.ORCID http://orcid.org/0000-0001-7826-3888
Memorial Sloan Kettering Cancer Center · USOregon Health & Science University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Identifying and Targeting Metabolic Dependencies in the Pancreatic Tumor MicroenvironmentR01CA229580 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Mara H. Sherman · 2018 to 2026
$3.8M
NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA069533NCI NIH HHS R01 CA229580
6 · The paper itself

Abstract

Lipids and their modifying enzymes regulate diverse features of the tumor microenvironment and cancer progression. The secreted enzyme autotaxin (ATX) hydrolyzes extracellular lysophosphatidylcholine to generate the multifunctional lipid mediator lysophosphatidic acid (LPA) and supports the growth of several tumor types, including pancreatic ductal adenocarcinoma (PDAC). Here we show that ATX suppresses the accumulation of eosinophils in the PDAC microenvironment. Genetic or pharmacologic ATX inhibition increased the number of intratumor eosinophils, which promote tumor cell apoptosis locally and suppress tumor progression. Mechanistically, ATX suppresses eosinophil accumulation via an autocrine feedback loop, wherein ATX-LPA signaling negatively regulates the activity of the AP-1 transcription factor c-Jun, in turn suppressing the expression of the potent eosinophil chemoattractant CCL11 (eotaxin-1). Eosinophils were identified in human PDAC specimens, and rare individuals with high intratumor eosinophil abundance had the longest overall survival. Together with recent findings, this study reveals the context-dependent, immune-modulatory potential of ATX-LPA signaling in cancer.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsChemokine CCL11EosinophilsHumansLysophosphatidylcholinesNeoplastic ProcessesTumor MicroenvironmentCCL11 protein, humanChemokine CCL11Lysophosphatidylcholines

Identifiers

PMID38195933
PMCPMC10899115
OpenAlexW4390706630

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.